Heparin-Induced Thrombocytopenia: A Focus on Thrombosis.
Heparin-Induced Thrombocytopenia: A Focus on Thrombosis.
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DOI：
10.1161/atvbaha.120.315445
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发表时间：
2021-01
期刊：
影响因子：
--
通讯作者：
Padmanabhan A
中科院分区：
文献类型：
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作者：
Arepally GM;Padmanabhan A
肝素诱导的血小板减少症（HIT）是一种免疫介导的疾病，由识别血小板因子4和肝素复合物的抗体引起。血栓形成是该综合征的中心和不可预测的特征。尽管有最佳的管理，血栓形成的疾病发病率和死亡率仍然很高。HIT的高凝状态在生物学上与其他血栓性疾病不同，因为临床并发症直接归因于循环超大免疫复合物（ULIC）。在某些个体中，ULIC引起未受抑制的细胞促凝反应，最终导致血栓形成。迄今为止，与HIT血栓形成风险相关的临床和生物学风险因素仍然难以捉摸。本文将总结我们目前对HIT血栓形成的认识，并关注其临床特征，细胞机制及其管理。
Heparin induced thrombocytopenia (HIT) is an immune mediated disorder caused by antibodies that recognize complexes of platelet factor 4 and heparin. Thrombosis is a central and unpredictable feature of this syndrome. Despite optimal management, disease morbidity and mortality from thrombosis remain high. The hypercoagulable state in HIT is biologically distinct from other thrombophilic disorders in that clinical complications are directly attributable to circulating ultra-large immune complexes (ULICs). In some individuals, ULICs elicit unchecked cellular procoagulant responses that culminate in thrombosis. To date, the clinical and biologic risk factors associated with thrombotic risk in HIT remain elusive. This review will summarize our current understanding of thrombosis in HIT with attention to its clinical features, cellular mechanisms, and its management.